Sleep Flashcards
Less than 7 hrs of sleep (short sleep duration) risk factors
Obesity
Smoking propensity
Heart attack/cardiovascular association
Depression
Diabetes
sleep deprivation experiments
Rats put on electrical wheel turned on whenever they start going into non-REM sleep
Food intake over days of sleep deprivation goes up
Drop in body weight despite eating more
Fail to control food intake and body temperature
Ultimately leads to death
circadian rhythms
rhythms that evolve over a 24 hr cycle
Sleep as an example of a circadian rhythm
Are endogenous
Regulated by external cues
Zeitgeber
Any stimulus that sets the clock
Ex: light/dark cycle
Food intake
Screen time (light)
Aging/developmental stage
Suprachiasmatic nucleus (SCN)
Group of 200k neurons in hypothalamus controlling many circadian rhythms
source of circadian rhythms (biological clock; endogenous)
lesions to scn causes
Lesions to SCN interfere with circadian rhythms
Activity becomes arrhythmic in hamster
What happens in the SCN to make the circadian rhythm tick?
Ex: drosophila have gene expression called period (per). If they have a mutation that disabled this gene, they have arrythmic gene expression in constant dim light. Clock wasnt running
Genes providing molecular clock
clock/cycle proteins and per/cry genes
- Cells in SCN make 2 proteins: Clock & Cycle
(Cycle —> Bmal-1 in mammals) - Promote transcription of per & cry genes
- Per and Cry dimerize and inhibit Clock/Cycle
- Slows transcription of per & cry genes
- Slow production of Per and Cry proteins
- Per / Cry eventually degrade with time, allowing Clock/Cycle to again promote per & cry transcription
→ Negative feedback loop
* Cycle takes 24 hrs
Ganglion cell than affect SCN: Retinohypothalamic tract
Projection of retinal ganglion cells that carries info about light-dark cycle to SCN
Intrinsically photosensitive retinal ganglion cells (ipRGC):
Form different pathway that goes directly to SCN
Are sensitive to light/dark bc of photopigment (melanopsin)
Do not respond to input from rods or cones
Glutamate released from RGP cells. It influences signal transduction and promotes production of period (per) protein.
Interferes with clock and can influence its timing
Why did sleep evolve?
Energy conservation (smaller mammals with higher metabolic rate sleep more)
Restorative function for body and brain
Clearance of metabolic waste (brain gets smaller and more blood flow and cerebral spinal fluid happens)
Glymphatic system clears out cellular waste coordinated in CNS with glia
Memory consolidation
At synaptic level: sleep helps reset weakened synapses not strengthened by experience
“Rehearse” information learned before onset of sleep through reactivation. Same pattern in awake stage is rehearsed and seems to reactivate memory
Disrupted sleep —> lack of clearance —> greater risk of neurodegenerative disorders
SCN and slave oscillators
Slave oscillators, also known as peripheral oscillators, are secondary oscillators located in other regions of the body, such as the liver, kidneys, and lungs. These oscillators are synchronized to the master pacemaker in the SCN and help maintain the body’s circadian rhythms in various tissues and organs.
The SCN sends signals to slave oscillators through various pathways, including the autonomic nervous system and hormonal signals, to coordinate the timing of various physiological processes. For example, the SCN may send signals to the pineal gland to regulate the release of the hormone melatonin, which helps regulate sleep-wake cycles.
Slave oscillators also send feedback signals back to the SCN, providing information on the local state of circadian rhythms in peripheral tissues. This feedback helps the SCN adjust its timing signals to maintain synchronization between the master pacemaker and peripheral oscillators.
Neural mechanisms of REM sleep: Pons
Pons is the source of REM signal
- Cortical activation
Cholinergic neurons in pons send activated signal to the rest of the brain via thalamus and basal forebrain which leads to desynchronized EEG of REM
- Spinal motor neuron inhibition
Glutamatergic neurons in pons inhibit spinal motor neurons → muscle atonia
Neural mechanisms of REM sleep: Hypothalamus
Hypocretins: neuropeptides produced in hypothalamus involved in switching between sleep states
prevent transition from wake directly to REM
what happens if hypocretin neurons are lost
If neurons lost, leads to narcolepsy
Humans with narcolepsy lost majority of hypocretin neurons (90%)
Aberrant activation of cataplexy pathway normally restricted to REM sleep
